controversial consequence of this view is that we may need to reexamine previously ascribed relationships between CNS development and attributes of motor control development.

For example, in a study correlating anatomy with behavior, spinal motoneuron dendrites were first observed at 12 postnatal days. The first-day kittens exhibited locomotion and reciprocal inhibition of antagonist muscles, leading the authors to suggest central programs for hindlimb activity may be generated by these dendritic bundles (Scheibel and Scheibel, Exp Neurol 1970). However, data from a series of studies on the development of locomotion, scratching and paw-shaking in normal kittens and littermates with spinal transections (T12), suggests that adult- like muscle patterns for these behaviors are established very early in development, prior to the emergence of corresponding behaviors (Bradley and Smith, Dev Bruin Res, 1988). Further, comparisons between normal and spinal littermates indicate that descending influences may initially inhibit expression of coor- dinated limb actions for these behaviors until postural require- ments are met. Most notably, in the absence of descending regulation of lumbosacral networks, spinal kittens exhibit hindpaw-shaking prior to both fore- and hindpaw shaking in normals. However, lacking control of the trunk and legs to generate stabilizing reaction forces, spinal kittens, in comparison to normals, exhibit significant delay in the onset of forepaw- shaking. In sum, postural requirements appear to delay the onset of hindpaw-shaking in normal kittens, whereas postural require- ments appear to delay the onset of forepaw-shaking in spinal littermates.

Recently, we began to test directly the hypothesis that postural requirements may be rate-limiting during motor development by studying the kinematics of motility in normal and spinal chicks in ovo. Chick embryos are known to produce orderly patterns of muscle activity during motility by embryonic day nine, yet classic behavioral studies indicate motility lacks coordination until the onset of hatching at the end of the embryonic period. One possible explanation for this apparent paradox is that reac-

tion forces emerging during movement under buoyant conditions in ovo perturb ongoing movements. Based on preliminary find- ings in embryos posturally stabilized, linear trends indicate that intralimb joint excursions (i.e. shoulder vs elbow) are closely related (r2 per cycle period can vary from approximately 0.6 to 0.8). Interlimb comparisons (i.e. shoulder vs. hip) indicate joint excursions are weakly related (1-2 of approximately 0.3) in nor- mal embryos, where as in spinals, excursions in the wing appear independent of the those in the leg (1-2 varying around 0.0). Further work is underway to determine whether theses relation- ships vary with changes in buoyancy (Chambers and Bradley, Soc Neurosci, 1992). This work was supported by FCAR, NSERC and the McGill Faculties of Graduate Studies and Medicine.

Set and Gain Control of Posture In Cerebellar and Vestibular Patients Fay B. Horak R.S. Dow Neurological Sciences Institute Of Good Samaritan Hospital Portland, Ore.

o maintain equilibrium, postural responses to sudden dis- T placements must be appropriately scaled to the speed and the size of the center of body mass displacement over the base of support. Previous studies have shown that, since postural respon- ses are usually initiated before peripheral information concem- ing the size of displacement becomes available, scaling initial responses to displacement amplitude depends upon expectation based on prior experience.

This central set results in increased or decreased responses, depending upon the expected stimulus amplitude. In contrast, stimulus velocity information is available within 75 ms of dis- placement onset, and so scaling initial responses to displacement velocity depends primarily upon peripheral feedback. However,

a, 3 e e

0 10 20 30 Veloci ty(cm/sec)

180

6 0 ' . ' - . 0 3 6 9 1 2

Amplitude (cm)

Left: Normal scaling, despite enlarged postural responses, to displacement velocity feedback by cerebellar and vestibular patients. Right: Inability of cerebellar, but not vestibular

patients, to scale responses to predicted displacement amplitudes. The group mean and standard deviations of the slope of the linear regressions are given.

December 1992 IEEE ENGINEERING IN MEDICINE AND BIOLOGY 95

expectation of stimulus velocity can also show effects of prior experience. Exposure to novel stimulus velocities results in enhanced responses with a gradual response reduction with repeated exposure.

We have proposed separate neural mechanisms for these two effects of prior experience: 1) adaptive central set, in which a default value, used for unexpected situations, is tuned up or down depending on the characteristics of immediate prior displace- ments and 2) local synaptic plasticity, resembling sensitization when a novel stimulus occurs and habituation with repeated exposure. Postural and gait ataxia are common motor control disorders accompanying cerebellar and vestibular dysfunction. Since vestibular information interacts with somatosensory and visual signals to provide sensory feedback to posture, and the cerebellum has been hypothesized to be involved in integration of these senses for adaptive gain control, we wondered whether these forms of ataxia might be associated with an inability to appropriately scale the magnitude of postural movements, either using peripheral feedback or based on prior experience.

Methods: By examining responses to five predictable ampli- tudes of surface displacement (backward direction, constant velocity), we tested the ability to scale postural responses using central predictive mechanisms. By examining responses to four different displacement velocities (backward direction, constant amplitude), we tested the ability to scale postural responses using peripheral sensory feedback. Response magnitude was quan- tified as the initial (first 75 ms) rate of change of surface torque response and plotted as a function of displacement amplitude or velocity to determine whether cerebellar or vestibular loss al- tered postural response gains. Responses of six patients with bilateral vestibular loss were compared with nine cerebellar patients with anterior lobe signs, and with 10 healthy control subjects with similar mean ages and weights.

Results: The vestibular and cerebellar patients had two to three

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96

times larger postural responses for all displacement amplitudes and velocities than normal subjects. Despite this increase in response bias, the vestibular patients had normal torque response/stimulus velocity or amplitude relationships (see fig- ure, left). In contrast, cerebellar patients showed normal scaling to stimulus velocity but were unable to scale to predicted stimulus amplitudes (see figure, right).

Discussion: The large magnitude of automatic postural respon- ses in patients with either bilateral vestibular loss or anterior lobe cerebellar degeneration suggests an increased gain of somatosen- sory loops which may contribute to their ataxia of gait and posture. Normal subjects modify the gain of their postural responses depending upon the anticipated amplitude of displace- ment. The magnitude of normal postural responses are gradually tuned to stimulus characteristics with practice using central set.

These studies suggest that such gain modification based on central set depends upon the anterior lobe of the cerebellum. It also suggests that this gain modification is accomplished by modifying the bias, but not the slope of the relation between response magnitude and stimulus characteristics. In cerebellar patients, Purkinje cell loss may result in disinhibition of somatosensory loops for postural control. In vestibular patients, the cerebellum may be involved in increasing somatosensory loop gains to compensate for vestibular loss.

It appears that neither the cerebellum, nor the vestibular system is critical for scaling postural responses to stimulus velocity using peripheral sensory information or for response sensitiza- tion and habituation. Perhaps, long latency somatosensory path- ways in the spinal cord and brainstem can accomplish velocity scaling and local habituation despite increased loop gains. The cerebellum appears to be critical for adaptive central set in which the gain of somatosensory-triggered postural responses are tuned to sensory conditions which are expected based upon prior experience.

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Ljubljana Functional Electrical Stimulation Conference Ljubljana, Slovenia

August 2-6, 1993

August 8-12, 1993

August 22-26, 1993

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Contact: Dr. Uros Stanic, J. Stefan Institute, Jamova 39,61000 Ljubljana, Slovenia. Tel: 38 61 159 199. Fax: 38 61 161 029

August 25-September 2, 1993 International Union of Radio Science: XXIVth General Assembly and Exhibition Kyoto, Japan Contact: Prof. I. Kimura, Center for Academic Societies Osaka, 14th Floor, Senri Life Sciences Building, 1-4-2 Shin- senri Higashi-machi, Toyonaka, Osaka 565, Japan. Tel: +81-6-873-2301. Fax: +8 1-6-873-2300

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December 1992